Primary Biliary Cholangitis, Primary Sclerosing Cholangitis, and Viral Hepatitis Flashcards
Path and CM of PBC
AI destruction…B and T cells…anti-mito ABs against E2 subunit or pyruvate dehydroganse
Most are asx but can get hepatomegaly….with dz progression, can get comps including hyperpgi, xanthelasms, and vit D malapsorption
Most common initial is alk phos elevation with maybe elevate transmaminases….about half will get hypercholesteroelmai
Ass with other AI dzs
Dx and managmeent of PBC
Elevated alk phos without ev od extrahepatic obstruction - middle aged women with mos of pruritis, fatigue and jaundice…elevated alk phos should have US
If alk phos and inc and US normal, get antimito AB measured
Can get liver biopsy as well - patchy destruciton of bile ducts in portal tracts…tracts surrounded by lymphocytic inflammatio nto form grandulomatous rxn centered on bile duct
Initial managmenet is therapy to delay destruction - ursodeoxycholic acid reduces secretion of cholesterol in bile and improves cholestasis
PSC path
Mediated injury to the bile ducts
Inflamm surrounds large bile ducts with neutros and lymphos
INflmaed areas result in fibrosis and strictures…will alternate between dilation and stricture
PSC CM/dx/comps/mg
Most asx but can get constitution sx
Most common presnetation is elevation in alk phos with or without elevation of milirubin
Dx - suspect in pts with IBD with elevated alk phos…get MRCP or ERCP….string or pearlys
Comps - Vit def, cholangiocarcinoma
Rapid pregression….ursodeoxycholic acid can dec secretion of cholesterol in bile….can get endoscopic dilation
Annual screening with US or MRCP to look for cholangiocarcinoma
Hep A, Hep B, Hep C, D, and E
A - single strand RNA, naked, fecal-oral, 2-6 incubation, no chornic
B - dsDNA, enveloped, parenteral/sexual contact, 2-26 week incubation, some chornic
C - single strand RNA, enveloped, parenteral, 4-26 week incubation, most chronic
D - single strand RNA, enveloped (Hep B), parenteral, same as HBV, vairable
E - ssRNA, naked, fecal oral, 4-5 week incubation, no chronic
Pathof hep
Viruses enter cells but do not destroy…CD4 T cells initiate immune response…CN8s play most role in clearing cells and pathogenesis
Lymphoplasmocytic mediated by CD4 is mostly in hepatic parenchyma with destruction of infection cells - spotty necrosis…portal tract is spared and developd scant infiltates…..ballooning degeneraion will occur with apoptotic cells….collagen framework collapses leading to cholestasis
Chonic - dense mononuclear infiltrate centered on portal tracts…fibrosis around portal tracts and septa form….B - ground glass and C shows scattered hepaticyte
Acute asx with recovery
Acute sx infection
Cold-like sx and hepatic infection never recognized…Hep A and B during chilhood…Hep C almost always asx
Prodromal illness that can be variable…more fever with A and E….cons sx improve in a week or 2 with GI sx….elevation of AST and ALT with bilirubin later
Acute fulminant hep
Chronic hep
Small percentage get hepatic fialure due to massive hpatic necoriss
Chronic more with hep C
Hep A CM
Occassional morbidity and rare moretality
Mildly sx and self-limited
In children - subclinial,
Adult - more likely to get sx
Jaundice peaks in 2 weeks….as illness progresses, dark urine, acholic stools and jaundice
Dx from anti-HAV IgM ABs in the stool
Hep B - repliaction
After host enters hepatocyte, DNA moves to nucleus where ti forms closed circular DNA….uses RNA polymerase of host…viral RNA transferred to cytoplasm where RNA is encapsulte into a viral core….mRNA forms template for DNA synthesases and get a neg DNA strand…using reverse transcriptase and neg strand template, a pos strand crrated….DNA core buds into intracellular membrane
Hep B dx
HBs - heb B surface antigen formed by envelops GPs
HBc - hep B nucelocpasid core protein
HBe - associated with active viral rep
HBsAG appears prior to onset of sx, ABs do not develop until after the acute infection
HBe rises soon after HBs and sinifies active rep….if continued production, then will become chronic
HBc - remains within hepatocytes and is not detectable in the blood…BUT the anti-HBc IgM is detectable shortly after onset of sx….if gap between HBsAg disppearace and anti0HBs AB, anti-HBc IgM may be onley detectable sign
HBc - regardless of severity or chornicity
Mg of He B
Tenofovir Entecavir IFN alpha Lamivudine Adefovir Telbivudine
Most with acute - conservatively
If worse - antivirla
Tenp - RT inhibt…1st line with rare resistance…contra if renal probs….effective if HIV
Ent - nucleoSIDE RT inhib….DOC with renal impairment
IFN - nhibit viral rep…atach of polyeth glycol reduces renal clearance….contraind if decomp
Lami - nucleoside RT inhib…exclusively if co-infected with HIV
Ade - TIDE RT inhibi - rarely used
Telbivudine - SIDE RT inhibt
Hep C CM and dx
Chronic - asx with fluctuating levels of ALT
Screening - pts on chronic hemodialysis, clotting factors before 1987, organ transplant befroe 1992
anti-HCV antibody can indicate past exposure or ongoing infection….followed by HCV RNA PCR
In acute, ABs only presenti n 50% so if acute get both PCR and ABs
Mg of Hep C
Type 1 - ledipasivr 9NS5A inhib and sofosbuvir (NS5B NA poly inhib) - 1st line
Also omvitasvir-pariaprevir and ritonavir (NS5A inhib-protease inhib with dasabuvir (NS5B RNA poly inhib)
Simepravir (protease) and sofosbuvir (RS5B RNA poly inhibt)
Type 2 and 3 - Sofosbuvir (NS5B RNA poly) and velpatasvir (NS5A inhibt)
Hep D
Only a neg ssRNA that does not encode surgface proteins
Needs HBV and HBsAg to envelope virus for dissemintation
Indistinguihsable from HBV alone
